妊娠期高血压(HDCP)是妊娠期的特发疾病,以妊娠20周后出现高血压、水肿、蛋白尿为主要表现的全身各器官和系统损害的一种妊娠期并发症,严重影响母婴健康,是孕产妇和围生儿患病及死亡的主要原因之一[1,2].降压治疗是HDCP的重要治疗手段,目的是预防子痫、心脑血管意外和胎盘早剥等严重母胎并发症,保证母儿安全,有效改善妊娠结局.我国2015年HDP诊治指南[3]参考了国际指南并结合我国国情建议:收缩压≥160 mmHg和(或)舒张压≥110 mmHg(1 mmHg=0.133 kPa)给予降压药物治疗,目标血压控制在130~155/80~105 mmHg,合并器官功能损伤,应控制130~139/80~89 mmHg,降压过程应平稳,避免过度波动,且血压不应低于130/80 mmHg,以保证子宫-胎盘的血流灌注[4].
To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague–Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.
Tanshinone IIA (Tan IIA) possesses potent anti-atherogenic function, however, the underlying pharmacological mechanism remains incompletely understood.Previous studies suggest that oxidized LDL (oxLDL)-induced NLRP3 (NOD-like receptor (NLR) family, pyrin domain-containing protein 3) inflammasome activation in macrophages plays a vital role in atherogenesis.Whether the anti-atherogenic effect of Tan IIA relies on the inhibition of the NLRP3 inflammasome has not been investigated before.In this study, we found that Tan IIA treatment of high-fat diet fed ApoE-/-mice significantly attenuated NLRP3 inflammasome activation in vivo.Consistently, Tan IIA also potently inhibited oxLDL-induced NLRP3 inflammasome activation in mouse macrophages.Mechanically, Tan IIA inhibited NF-κB activation to downregulate pro-interleukin (IL) -1β and NLRP3 expression, and decreased oxLDLinduced expression of lectin-like oxidized LDL receptor-1 (LOX-1) and cluster of differentiation 36 (CD36), thereby attenuating oxLDL cellular uptake and subsequent induction of mitochondrial and lysosomal damage -events that promote the NLRP3 inflammasome assembly.Through regulating both the inflammasome 'priming' and 'activation' steps, Tan IIA potently inhibited oxLDL-induced NLRP3 inflammasome activation, thereby ameliorating atherogenesis.
OBJECTIVE:To investigate whether exercise preconditioning (EP) improves the rat cardiac dysfunction induced by exhaustive exercise (EE) through regulating NOD-like receptor protein 3 (NLRP3) inflammatory pathways and to confirm which intensity of EP is better.METHOD:Ninety healthy male Sprague Dawley rats were randomly divided into five groups: a control group (CON), exhaustive exercise group (EE), low-, middle-, and high-intensity exercise precondition and exhaustive exercise group (LEP + EE, MEP + EE, HEP + EE group). We established the experimental model by referring to Bedford's motion load standard to complete the experiment. Then, the pathological changes of the myocardium were observed under a light microscope. Biomarker of myocardial injury in serum and oxidative stress factor in myocardial tissue were evaluated by ELISAs. The cardiac function parameters were detected using a Millar pressure and volume catheter. The levels of thioredoxin-interacting protein (TXNIP), thioredoxin protein (TRX), nuclear transcription factor kappa Bp65 (NF-ĸBp65), NLRP3, and cysteinaspartate specific proteinase 1 (Caspase-1) protein in rats' myocardium were detected by western blotting.RESULTS:1. The myocardial structures of three EP + EE groups were all improved compared with EE groups. 2. The levels of the creatine phosphating-enzyme MB (CK-MB), reactive oxygen species (ROS), interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor alpha (TNF-α) in three EP + EE groups were all increased compared with CON but decreased compared with the EE group (P < 0.05). 3. Compared with the CON group, slope of end-systolic pressure volume relationship (ESPVR), ejection fraction (EF), and peak rate of the increase in pressure (dP/dt max) all dropped to the lowest level in the EE group (P < 0.05), while the values of cardiac output (CO), stroke volume (SV), end-systolic volume (Ves), end-diastolic volume (Ved), and relaxation time constant (Tau) increased in the EE group (P < 0.05). 4. Compared with the CON group, the expression levels of TXNIP, NF-ĸBp65, NLRP3, and Caspase-1 all increased obviously in the other groups (P < 0.05); meanwhile, they were all decreased in three EP + EE groups compared with the EE group (P < 0.05). 5. NLRP3 was positively correlated with heart rate, IL-6, and ROS, but negatively correlated with EF (P < 0.01).CONCLUSION:EP protects the heart from EE-induced injury through downregulating TXNIP/TRX/NF-ĸBp65/NLRP3 inflammatory signaling pathways. Moderate intensity EP has the best protective effect.
Listeria monocytogenes (LM), a foodborne pathogen, can cause pregnancy failure in animals, especially in ruminants. Recent studies have shown that LM activates inflammasomes to induce IL-1β release in macrophages, however, whether the inflammasome activation regulates LM-induced pregnancy failure remains largely unknown. Here we used mouse model to investigate the molecular mechanism by which LM-induced inflammsome activation contributes to LM-associated pregnancy failure
Objective To investigate the expressions and mutual relationship of Galectin-3 andβ-catenin in endome?triosis (EM). Methods Immunohistochemistry was used to detect expression levels of Galectin-3 andβ-catenin and their mutual relationship in expression was also examined. Samples were collected from ectopic endometrium of patients with en?dometriosis (ectopic endometrium group, n=34), eutopic endometrium of patients with endometriosis (eutopic endometrium group, n=34) and normal endometrium from people without endometriosis (control group, n=30). Results The expressions of Galectin-3 were seen in 88.2%, 85.3%, 50.0%of cases in ectopic endometrium group, eutopic endometrium group and control group respectively. On the other hand, the expression ofβ-catenin were seen in 55.9%, 52.9%, 26.7%of cases in ecto?pic endometrium group, eutopic endometrium group and control group respectively. In EMs patients, the expression of Galec?tin-3 andβ-catenin were significantly higher in ectopic endometrium and eutopic endometrium than those in normal endome?trium group(P<0.05). Expression of Galectin-3 was positive correlated with expression ofβ-catenin(rs=0.512, 0.428, P<0.01). Conclusion Galectin-3 andβ-catenin may play important roles synergistically in the pathogenesis of endometriosis.
目的 建立心复康口服液的质量评价方法.方法 采用薄层色谱法对心复康口服液中的主要药味黄芪、人参、丹参、淫羊藿进行定性鉴别,并对其中的有毒药味附子进行乌头碱的限量检查;在此基础上,采用高效液相色谱法对方中君药人参的指标成分人参皂苷Rg1进行线性关系考察和稳定性、精密度、重现性、回收率试验,并测定批号为20080406、20080527、20080618共3批心复康口服液中人参皂苷Rg1的含量.结果 薄层色谱法显示,心复康口服液中含有黄芪、人参、丹参、淫羊藿;有毒物质限量检查可知乌头碱在规定的剂量范围.人参皂苷Rg1在194.4~5832.0 ng范围内呈良好的线性关系;同一批供试品8h内峰面积的相对标准偏差(RSD)为1.58%,表明药物基本稳定;同一份人参皂苷Rg1峰面积的RSD为0.41%,表明精密度良好;同一批样品人参皂苷Rg1峰面积的RSD为0.07%,表明本法重现性良好;人参皂苷Rg1的平均加样回收率为98.70%,RSD为1.71%.批号为20080406、20080527、20080618心复康口服液人参皂苷Rg1的含量分别为61.37、57.60、42.27μg/ml,RSD为0.90%、1.40%、1.90%.结论 本研究中建立的质量评价系统能够有效反映心复康口服液的质量,可作为评价心复康口服液质量的有效手段.
子宫内膜异位症(EMs)是严重影响中青年妇女健康和生活质量的多发病、常见病,其发病机制复杂不明确.1921年,Sampson提出经血种植逆流学说,但该学说无法解释90%育龄妇女经血逆流却只有10%~15%患EMs.